Correction and Retraction CORRECTION PHYSIOLOGY Correction for “Deletion of claudin-10 (Cldn10) in the thick ascending limb impairs paracellular sodium permeability and leads to hypermagnesemia and nephrocalcinosis,” by Tilman Breiderhoff,
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PHYSIOLOGY Correction for “Deletion of claudin-10 (Cldn10) in the thick ascending limb impairs paracellular sodium permeability and leads to hypermagnesemia and nephrocalcinosis,” by Tilman Breiderhoff, Nina Himmerkus, Marchel Stuiver, Kerim Mutig, Constanze Will, Iwan C. Meij, Sebastian Bachmann, Markus Bleich, Thomas E. Willnow, and Dominik Müller, which appeared in issue 35, August 28, 2012, of Proc Natl Acad Sci USA (109:14241–14246; first published August 13, 2012; 10.1073/ pnas.1203834109). The authors note that, due to a printer’s error, Table 1 appeared incorrectly. This error does not affect the conclusions of the article. Both the online article and the print article have been corrected.
منابع مشابه
Claudin Loss-of-Function Disrupts Tight Junctions and Impairs Amelogenesis
Claudins are a family of proteins that forms paracellular barriers and pores determining tight junctions (TJ) permeability. Claudin-16 and -19 are pore forming TJ proteins allowing calcium and magnesium reabsorption in the thick ascending limb of Henle's loop (TAL). Loss-of-function mutations in the encoding genes, initially identified to cause Familial Hypomagnesemia with Hypercalciuria and Ne...
متن کاملRenal localization and function of the tight junction protein, claudin-19.
Claudins form a family of transmembrane tight junction proteins that play a key role in control and selectivity of paracellular transport. Mutations in claudin-19, which is expressed in kidney, retina, and myelinated peripheral neurons, were identified in familial hypomagnesemia with hypercalciuria and nephrocalcinosis, a hereditary disease causing renal Mg(2+) and Ca(2+) wasting. Here, we stud...
متن کاملSalt and acid-base metabolism in claudin-16 knockdown mice: impact for the pathophysiology of FHHNC patients.
Claudin-16 is defective in familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). Claudin-16 knockdown (CLDN16 KD) mice show reduced cation selectivity in the thick ascending limb. The defect leads to a collapse of the lumen-positive diffusion voltage, which drives Ca(2+) and Mg(2+) absorption. Because of the reduced tight junction permeability ratio for Na(+) over Cl(-), we ...
متن کاملClaudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium.
Claudins are tight junction integral membrane proteins that are key regulators of the paracellular pathway. Defects in claudin-16 (CLDN16) and CLDN19 function result in the inherited human renal disorder familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). Previous studies showed that siRNA knockdown of CLDN16 in mice results in a mouse model for FHHNC. Here, we show that C...
متن کاملParacellin-1 and the modulation of ion selectivity of tight junctions.
Tight junctions play a key selectivity role in the paracellular conductance of ions. Paracellin-1 is a member of the tight junction claudin protein family and mutations in the paracellin-1 gene cause a human hereditary disease, familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) with severe renal Mg2+ wasting. The mechanism of paracellin-1 function and its role in FHHNC are...
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تاریخ انتشار 2012